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  1. #11
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    Oxidants cause oxidative stress. Now that is clear, I want to explain why oxidants can regrow hair. There are two primary reasons why oxidants can regrow hair:

    1) Oxidants can decrease proteasome degradation. Therefore, it can act a Proteasome inhibitor. Remember that people in the past have used Proteasome inhibitors topically and grew hair.
    2) Oxidants can inhibit p16 senescence. P16 activation is directly involved with the balding dermal papilla. This means that if you inhibit p16 the balding process will stop with the possibility of regrowth.

    Oxidants cause oxidative stress. Therefore they can cause damage. If you do not know what oxidative stress is, please read about it. Using them may be more harmful than good if you do not know how to use an oxidant properly for hair loss.

    I urge all of you to do some research for yourself. Do a searches with oxidative stress and proteasome and another search with oxidative stress and p16. Use google, google scholar, and PubMed.

    The key for oxidants to work is dose and time (cycling). This needs to be experimented with.

    There are two oxidants that have been discussed with no explanation as to why they can work for hair loss. Now we know the scientific reason why oxidants can cause hair to regrow. Those oxidants were:

    1) Chlorine Dioxide
    2) Miconazole Nitrate (nitrates cause oxidative stress)

    Hope this helps.

  2. #12
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    Quote Originally Posted by AnteUp View Post
    Oxidants cause oxidative stress. Now that is clear, I want to explain why oxidants can regrow hair. There are two primary reasons why oxidants can regrow hair:

    1) Oxidants can decrease proteasome degradation. Therefore, it can act a Proteasome inhibitor. Remember that people in the past have used Proteasome inhibitors topically and grew hair.
    2) Oxidants can inhibit p16 senescence. P16 activation is directly involved with the balding dermal papilla. This means that if you inhibit p16 the balding process will stop with the possibility of regrowth.

    Oxidants cause oxidative stress. Therefore they can cause damage. If you do not know what oxidative stress is, please read about it. Using them may be more harmful than good if you do not know how to use an oxidant properly for hair loss.

    I urge all of you to do some research for yourself. Do a searches with oxidative stress and proteasome and another search with oxidative stress and p16. Use google, google scholar, and PubMed.

    The key for oxidants to work is dose and time (cycling). This needs to be experimented with.

    There are two oxidants that have been discussed with no explanation as to why they can work for hair loss. Now we know the scientific reason why oxidants can cause hair to regrow. Those oxidants were:

    1) Chlorine Dioxide
    2) Miconazole Nitrate (nitrates cause oxidative stress)

    Hope this helps.
    What about people like me who consume anti-oxidants on a daily basis (cup of green tea daily + fruit daily) and still deal with hairloss while many of my counterparts who eat the American diet (cheeseburgers, pizza, french fries) on a daily basis don't suffer from hairloss. Is it possible that they are less sensitive to alpha 5 reductase activity and type II dht? Maybe I'm drawing straws here.

  3. #13
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    Quote Originally Posted by cthulhu2 View Post
    What about people like me who consume anti-oxidants on a daily basis (cup of green tea daily + fruit daily) and still deal with hairloss while many of my counterparts who eat the American diet (cheeseburgers, pizza, french fries) on a daily basis don't suffer from hairloss. Is it possible that they are less sensitive to alpha 5 reductase activity and type II dht? Maybe I'm drawing straws here.
    indeed in vivo studies have shown that non mpb dermal papilla express less androgen receptors plus less 5ar reductase enzymes. transfecting the dps with AR receptor virus caused the non mpb dps to behave mpb like dps.

    anti oxidants can clearly slow down hairloss(atleast topically proper dose), however if we want regrowth we need to get rid of the aged cells by selectively damaging them. neither CD or dermarolling is selective.

  4. #14
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    The pros and cons of ROS (reactive oxygen species), STAT3, HIF1



    ROS:

    Pro: Normal levels allow for angiogenesis. This is true for the mitochondria.

    Cons:ROS created by mast cells is a problem we face in AGA. An up regulation in mitochondria causes apoptosis



    Studies say ROS can cause or inhibit apoptosis-sometimes no clear answer, but the above statements are true. The problem is what is causing ROS and the environment(apoptosis or angiogenesis)



    Stat3:

    Pro: Stat 3 and Hif 1 alpha allows for VEGF production.



    Cons:The problems is that STAT 3 is also involed with IL6 which is upregulated in AGA causing apoptosis. Also, STAT3 downregulates mitochondrial gene production, so it decreases its activity.



    HIF1

    CON:HIF causes a downregulation of the mitochondria to produce ROS



    PRO:HIF1 is involved with angiogenesis



    What I have noticed is that there is a cycle and particular environment which affects whether STAT3, ROS, HIF1 will cause apoptosis or angiogenesis. From what I noticed is some studies is that wounding causes angiogenesis in a time dependent manner expression involving ROS and HIF 1. I have said before, that cycling topicals to promote the hair follicle differentiation, proliferation, and eventual regrowth is something we need to really look into.





    Quick addition: HIF 1 alpha is in the cytoplasm of cells and HIF 1 beta in the nucleus. When they both combine they can cause angiogenesis. HIF 1 alpha in the cytosol under normal oxygen conditions is degraded by the ubiquitin proteasome pathway. This is why a proteasome inhibitor is important for hair growth. To allow angiogenesis (hair growth) under normal oxygen conditions in our scalp.



    NRF2 expression of antioxidants causes overexpression of the ubiquitin proteasome pathway-Another reason why it is important to inhibit NRF2





    My question: What is the mechanism or pathway in which Neogenic (stemoxydine) works?

  5. #15
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    I take Resverarol orally daily and I don't really know if it affects my hair in some way. Should I apply it topically?

    I like the extensive research here but what's the conclusion from all this? What do we do?

  6. #16
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    Quote Originally Posted by AnteUp View Post
    NRF2 expression of antioxidants causes overexpression of the ubiquitin proteasome pathway-Another reason why it is important to inhibit NRF2
    im not sure its what we want : increase NRF2 actually increase GSH wich is low in bald scalp..

  7. #17
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    I glanced over the Garza et al paper and I found out something interesting. AGA scalp has all the stem cells needed, but it is lacking only two progenitor cells: CD34 (aka CD34+) and CD200 (aka CD200hiTGA6hi). In an update to the thread I stated how wounding effects the hair follicle. When the scalp is wounded, Lhx2 is activated in the hair follicle. Lhx2 inhibits Lgr5 which regulates bulge and secondary germ stem cells. Inhibiting Lgr5 will keep hair in anagen by inhibiting stem cell activation.

    Here is the problem. Lgr5 is a marker for activated bulge and secondary hair germ cells. In the Garza et al study, they state that Lgr5 is reduced in bald scalp. Lgr5 is directly correlated with CD200hiITGA6hi cells (the cd200 cells that balding hairs lack). This means that we need to express Lgr5 in order to potentially regain the CD200 cells ( specifically CD200hiTGA6hi) that are lacking in androgenetic alopecia. What is interesting is that Lgr5 is considered as a tumor suppressor gene (Wikipedia).

    This should mean that while wounding may help keep your existing hair in anagen for a short duration (5-7 days) it is inhibiting Lgr5 which has been shown to be responsible for CD200 (CD200hiTGAGhi).

    If you have been wounding your scalp on a weekly basis, you are only keeping your terminal hair and thinning hairs that are not vellus in the anagen phase. This may be your cure if you have not receded or lost much hair; but be aware that suppressing Lgr5 for a long time and stopping wounding may have terrible consequences for your hair. Not to mention that long term wounding may lead to cancer. Lgr5 and CD200 is needed to form thick, terminal hair. I may have found one way to induce Lgr5/CD200. It would be nice if some of you can do some research and find potential other ways to do so. There needs to be some more medical research done on this as well.

    There are studies showing that low dose Reactive Oxygen Species (ROS/Oxidants) can cause JNK and Lgr5 activation. JNK and tcf4 (activated by wounding via Lhx2) work together in tumorgenesis. Remember I stated before that our hair follicles are being treated like a tumor/cancer and in order to get regrowth we need to promote tumor like pathways. This is starting to get interesting.

    Now for an update on CD34. The reason why Garza et al paper states that CD34+ is lacking is because of the decrease of the wnt/canonical pathway in AGA. In the thread where I made my second post, I said that I had discovered that TCF7 is directly involved with CD34. This is now a fact. Also, another fact is that when TCF7 is downregulated, CD34+ turn into CD34- cells. In order for us to increase CD34+ cells in the hair follicle, we need to activated the wnt canonical pathway and/or inhibit GSK3 Beta. A link below proves that LITHIUM can upregulate the proper type of TCF7 that will allow CD34+ cells to proliferate.

    People have used the following topically, often separately, with relative success: oxidants, lithium chloride, androgen receptor inhibitors, and wounding. Many have had some success with them, but no cure. The reason is because each one is lacking or inhibiting something critical for the regrowth of terminal hair. Here is where I believe we have a potential cure:

    Androgen Receptor Inhibition--stop the AGA pathway/cascade (inflammation, senescence, etc)
    Lithium Chloride--Induce the Wnt B-Catenin pathway and CD34+ progenitor cells
    Wounding--Induce anagen. Angiogenesis. Break fibrotic plaque. SOX9, Lhrx2, tcf4 hair follicle progenitor stem cell production
    Low dose ROS (oxidant like hydrogen peroxide)-- induce Lgr5/CD200/CD200hiTGA6hi

    This is what all 4 of the above should do--Regrowth of thick terminal hair

    Now the question is if we need to cycle these or can we use them together. I have tried my best to understand AGA, the hair cycle, and all the factors involved with hair loss. I try to understand most of the material I read, but I am no expert. This is where we need the medical research community to get involved.

    Inhibiting androgen receptors will cause the cessation of the androgenetic alopecia pathway of miniaturization, inflammation, and apoptosis . This is not a cure in itself because there has been senescent damage done to the androgen sensitive hair follicles. There are two types of damage. One is thinning of the hair follicle, but still retains the ability to grow. The other is miniaturization into vellus hairs. We have learned that we contain all the stem cells needed to regrow hair, but lack 2 progenitor cells (CD34 and CD200). Both of these cells are involved with the hair follicle cycle. Cd34 is more involved with anagen and CD200 with the diameter of the hair. We now have the potential to induce the proliferation of CD34 via lithium and CD200 via low dose ROS (hydrogen peroxide). Lithium and wounding will promote anagen. Wounding the scalp will allow (please read the 3 page pdf I posted a link to below) the other progenitor/stem cells proliferation involved with the hair follicle. Wounding will allow us to break fibrotic plaques and during healing will allow angiogenesis (blood vessels, etc) to take place; so that we can have the optimal environment for thick terminal hair. The low dose ROS oxidant should counteract the inhibition of Lgr5/CD200 during wounding.

    Not all my links are about the hair follicle. If you want more proof, do your own search. Better yet, start talking to potential medical researchers about this and see if they can verify it. I would like to see a future study regarding this idea. I believe if I can do a simple online search, reading articles, and finding information as what I wrote above, there can be a way to cure Androgenetic Alopecia. The sad truth is that there is no money involved in a cure; especially if it is as simple as what I posted above. The money is in hair transplants, synthetic medicines, topicals, and injections. If we were to fund our own research or if the medical community obliges to sincerely help, we can find a cure.

    Links:

    http://www.sciencedirect.com/science...92867411007562 (download the 3 page pdf)

    http://www.ncbi.nlm.nih.gov/pubmed/20654575

    http://www.plosgenetics.org/article/...l.pgen.1002565

    http://jcs.biologists.org/content/114/23/4329.full.pdf

    http://mcr.aacrjournals.org/content/7/8/1189.full

    http://www.pubfacts.com/detail/22923...signaling-path

    http://www.ncbi.nlm.nih.gov/pubmed/21206086

    http://www.jci.org/articles/view/44478

    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4067271/

  8. #18
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    anteup, your research is great.

    I think you'd get more help if you ended your posts with 1-2 sentences, bolded, that you consider next steps. Also, the tl;dr conclusion would be good.

    eg.


    TAKEAWAY: You have awesome posts, but need to finish strong in your conclusion/wrap up

    NEXT STEPS: You should edit takeaways/next steps into your past posts, and plan to use them in the future posts

  9. #19
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    The biggest barrier though is how do you apply that knowledge to safely and effectively achieve what you want? Twenty years later there are still few if any safe ways to actually inhibit the androgen receptors for instance even though we knew that for 20+ years. You say RU or CB but that fact is right now there are no proven ways to even do that safely. A lot of them get into grey areas of how effective is something at actually achieving that? I think turning the theory into practice is by far and away the most expensive and hardest part

    Androgen Receptor Inhibition--stop the AGA pathway/cascade (inflammation, senescence, etc)

  10. #20
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    Your research is great. I really have the hope that you/we can find something if we continue. Maybe there is already the cure based on these treatment ways but ofcourse the Pharma Companys are more interested in treatments which let them earn money over a long period of time such as fin or minoxidil. Keep on bro.

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